Detection of Gene Amplification in Archival Breast Cancer Specimens by Laser-Assisted Microdissection and Quantitative Real-Time Polymerase Chain Reaction

Lehmann, Ulrich; Glöckner, Sabine C.; Kleeberger, Wolfram; Wasielewski, Henning Feist Reinhard von; Kreipe, Hans

doi:10.1016/s0002-9440(10)65059-6

Cited by 128 publications

(95 citation statements)

References 36 publications

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“…Interestingly, IPH-926 and MDA-MB-134 both harbour a loss at 8p23 and a gain at 8p12-p11 ( Figure 7A). This was confirmed by quantitative gene dosage PCR for DLGAP2 at 8p23 and FGFR1 at 8p11 [30]. Based on quantitative gene dosage PCR, the FGFR1 gene copy number was clearly elevated in both IPH-926 and MDA-MB-134 ( Figure 7B).…”

Section: Comparison Of Iph-926 and Mda-mb-134mentioning

confidence: 53%

“…Laser microdissection and DNA extraction of tumour cells from FFPE tissue were performed with a PALM Laser-MicroBeam System and proteinase K digestion as described previously [30]. Allelic loss at the CDH1 locus was assessed with the microsatellite marker D16S752, which maps to 16q22 close to the CDH1 gene [3].…”

Section: Laser Microdissection and Loss Of Heterozygosity (Loh) Analysismentioning

confidence: 99%

“…Quantitative gene dosage PCR was performed essentially as described before [30]. Details of the reaction conditions, PCR primers and data evaluation are given in the Supporting information, Supplementary Methods.…”

Section: Quantitative Gene Dosage Pcrmentioning

confidence: 99%

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Comprehensive genetic and functional characterization of IPH‐926: a novel CDH1‐null tumour cell line from human lobular breast cancer

Christgen

Bruchhardt

Hadamitzky

et al. 2009

The Journal of Pathology

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Section: Comparison Of Iph-926 and Mda-mb-134mentioning

confidence: 53%

Section: Laser Microdissection and Loss Of Heterozygosity (Loh) Analysismentioning

confidence: 99%

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Comprehensive genetic and functional characterization of IPH‐926: a novel CDH1‐null tumour cell line from human lobular breast cancer

Christgen

Bruchhardt

Hadamitzky

et al. 2009

The Journal of Pathology

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“…The normal ductal epithelium and stroma were also examined. The microdissected tissue were applied into 60 L proteinase K-digestion buffer and incubated at 56°C overnight (5). The samples were centrifuged and the supernatants were treated at 95°C for 10 minutes.…”

Section: Microdissection and P53 Mutation Analysismentioning

confidence: 99%

Metaplastic Carcinoma of the Breast: p53 Analysis Identified the Same Point Mutation in the Three Histologic Components

et al. 2001

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A rare case of metaplastic carcinoma of the breast with both squamous metaplasia and cartilaginous metaplasia was reported. Histologically, the neoplasm revealed complex features, which were consisting of invasive ductal carcinoma, squamous carcinomatous component and chondrosarcomatoid component. Gradual transition of each component was recognized microscopically. p53 mutation analysis disclosed the same point mutation in three histologically different components, but not in the normal epithelium. Based on the morphologic findings, immunohistochemical findings and the p53 mutation analysis, we concluded that these three components in the tumor originated from the same duct progenitor cells. KEY WORDS: Breast cancer, cartilaginous metaplasia, Metaplastic carcinoma, p53, Squamous metaplasia.

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“…14,15 Recent studies using laser-assisted microdissection from tissue sections have provided an insight into the biology of not only different diseases, including breast cancer, 16 malignant lymphoma, 17 lung cancer 18 and pancreatic cancer, 19 but also normal skin. 20 In our study.…”

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confidence: 99%

p53 mutation profiling of multiple esophageal carcinoma using laser capture microdissection to demonstrate field carcinogenesis

Ito

Ohga

Saeki

et al. 2004

Intl Journal of Cancer

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Inactivation of the p53 tumor suppressor gene is one of the most frequent genetic alterations observed in human esophageal carcinomas. In patients with esophageal carcinoma, one of the significant pathological features of the tumor is the presence of multiple lesions within the esophagus. However, the molecular mechanisms involved in the occurrence of multiple lesions have remained elusive. To characterize p53 alterations in multiple esophageal carcinomas and to study their roles in carcinogenesis, we performed p53 immunohistochemical and p53 mutation analyses using laser capture microdissection on surgically resected human esophageal carcinomas from 11 patients: 9 patients with multiple esophageal carcinomas, 1 with an intramural metastasis lesion within the esophagus and 1 with an intraepithelial carcinoma lesion contiguous to the main lesion. In each of the patients with multiple esophageal carcinomas, we examined samples from 1 main lesion and 1 representative concomitant lesion. Molecular analyses of samples from fresh-frozen normal tissues and tumor tissues of the main lesion (whole tumor) were also performed by the same method. p53 protein accumulation was observed in 16 (72.7%) of 22 lesions from the 11 cases. No p53 mutation was found in normal esophageal tissues. In the 9 cases of multiple esophageal carcinomas, point mutations were detected in the whole tumor in 1 (11.1%) case, in the microdissected tumor samples of main lesions in 3 (33.3%) cases and in the microdissected tumor samples of concomitant lesions in 3 (33.3%) cases. For the microdissected tumor samples, there was a 54.5% (12/22) concordance rate between the results of immunostaining and molecular analysis. In the 8 cases of whole tumors in which a p53 mutation was not observed, 2 cases revealed p53 mutation in the microdissected tumor samples of the main lesion. All 6 cases of multiple esophageal carcinomas that showed a p53 mutation in the microdissected tumor sample had a discordant p53 mutational status between the main and concomitant lesions. In contrast, both the intramural metastasis lesion and the intraepithelial carcinoma contiguous to the main lesion showed p53 mutational patterns identical to those of the main lesions. In conclusion, the analysis of microdissected DNA by laser capture microdissection is useful for characterizing the heterogeneity of the p53 gene mutation in multiple carcinoma lesions that cannot be accurately analyzed in whole esophageal tumor DNA. The finding of different p53 gene mutations among multiple esophageal carcinoma lesions suggest further evidence of multicentric or field carcinogenesis of the human esophagus.

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Detection of Gene Amplification in Archival Breast Cancer Specimens by Laser-Assisted Microdissection and Quantitative Real-Time Polymerase Chain Reaction

Cited by 128 publications

References 36 publications

Comprehensive genetic and functional characterization of IPH‐926: a novel CDH1‐null tumour cell line from human lobular breast cancer

Comprehensive genetic and functional characterization of IPH‐926: a novel CDH1‐null tumour cell line from human lobular breast cancer

Metaplastic Carcinoma of the Breast: p53 Analysis Identified the Same Point Mutation in the Three Histologic Components

p53 mutation profiling of multiple esophageal carcinoma using laser capture microdissection to demonstrate field carcinogenesis

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